The Weight of Frailty in Neurosurgery Patients: Analyzing the Combined Effect of Frailty and Body Mass Index on 30-Day Postoperative Mortality.

OBJECTIVE: There is a rising prevalence of overweight and obese persons in the US, and there is a paucity of information about the relationship between frailty and body mass index. Therefore, we examined discrimination thresholds and independent relationships of the risk analysis index (RAI), modified frailty index-5 (mFI-5), and increasing patient age in predicting 30-day postoperative mortality. METHODS: This retrospective American College of Surgeons National Surgical Quality Improvement Program analysis compared all overweight or obese adult patients who underwent neurosurgery procedures between 2012 and 2020. We compared discrimination using receiver operating characteristic curve analysis for RAI, mFI-5, and increasing patient age. Furthermore, multivariable analyses, as well as subgroup analyses by procedure type i.e., spine, skull base, and other (vascular and functional) were performed, and reported as odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS: We included 315,725/412,909 (76.5%) neurosurgery patients, with a median age of 59 years (interquartile range: 48-68), predominately White 76.7% and male 54.3%. Receiver operating characteristic analysis for 30-day postoperative mortality demonstrated a higher discriminatory threshold for RAI (C-statistic: 0.790, 95%CI: 0.782-0.800) compared to mFI-5 (C-statistic: 0.692, 95%CI: 0.620-0.638) and increasing patient age (C-statistic: 0.659, 95%CI: 0.650-0.668). Multivariable analyses showed a dose-dependent association and a larger magnitude of effect by RAI: frail patients OR: 11.82 (95%CI: 10.57-13.24), and very frail patients OR: 31.19 (95%CI: 24.87-39.12). A similar trend was observed in all subgroup analyses i.e., spine, skull base, and other (vascular and functional) procedures (P ≤ 0.001). CONCLUSIONS: Increasing frailty was associated with a higher rate of 30-day postoperative mortality, with a dose-dependent effect. Furthermore, the RAI had a higher threshold for discrimination and larger effect sizes than mFI-5 and increasing patient age. These findings support RAI's use in preoperative assessments, as it has the potential to improve postoperative outcomes through targeted interventions.

Mechanisms and Treatment Options for Hyperthyroid-Induced Osteoporosis: A Narrative Review.

Normal thyroid hormone levels are crucial for the homeostasis of many metabolic cycles and processes throughout the human body. Thyroid dysfunction, such as thyrotoxicosis, can result from many different etiologies, including Graves' disease (GD), toxic multinodular goiter (MNG), and toxic adenoma. These hyperthyroid disease states can cause devastating complications and disease, including the disruption of the bone remodeling cycle and skeletal development, which can result in osteoporosis. Osteoporosis is characterized by a decrease in bone mineral density and a propensity for fragility fractures. In addition to patients with overt hyperthyroidism, studies have provided evidence of other high-risk patient demographics, such as individuals with subclinical hyperthyroidism and postmenopausal women, who may be at an increased risk for the development of secondary osteoporosis. The treatment of patients with hyperthyroid-induced osteoporosis often requires a multifaceted management plan that may be unique to each patient's situation. Antithyroid therapy is often the first step in treating this disease and may include thioamide medications. Radioactive iodine-131 therapy (RAI) and the surgical removal of the thyroid gland may also be reasonable approaches for restoring normal thyroid function. Following thyrotoxicosis mitigation, antiresorptive drugs such as bisphosphonates, calcitonin, and selective estrogen receptor modulators (SERMs) may be used to counteract decreased bone mineral density (BMD). Additionally, the implementation of vitamin D, calcium supplements, and weight-bearing exercise may also reduce bone loss. While the effects of thyroid stimulating hormone (TSH) and triiodothyronine (T3) on bone remodeling have been studied in the past, more research is needed to identify unknown mechanisms and develop future improved treatments for this condition.